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Pancreatic islet function in nondiabetic and diabetic BB rats
M Teruya1, S Takei, L E Forrest
1Department of Medicine, University of California, Irvine 92717.
Diabetes
|September 1, 1993
Summary
Inflammation in islets of diabetes-prone rats enhances insulin secretion, challenging the notion of intrinsic secretion defects in predicting diabetes onset.
Area of Science:
- Endocrinology
- Diabetes Research
- Islet Biology
Background:
- Decreased acute insulin response to glucose in humans with islet cell antibodies predicts diabetes.
- The underlying mechanisms for reduced in vivo insulin response remain unclear.
Purpose of the Study:
- To investigate the role of glucose sensitivity in insulin secretion by individual islets.
- To assess insulin secretion dynamics in diabetes-prone BB rats before and after diabetes onset.
Main Methods:
- Perifusion of isolated islets from normal WF rats, diabetes-prone rats (inflamed and non-inflamed islets), and diabetic rats.
- Measurement of insulin secretion at varying glucose concentrations (2.0, 8.3, and 16.7 mM).
Main Results:
- Diabetes-prone non-inflamed islets showed no intrinsic secretion abnormality compared to WF rats.
- Diabetes-prone inflamed islets exhibited significantly increased first and second-phase insulin secretion at 16.7 mM glucose compared to WF rats.
- Basal insulin secretion at 2 mM glucose was elevated in inflamed islets.
Conclusions:
- Inflammation in islets of diabetes-prone rats is associated with enhanced, not diminished, insulin secretion.
- These findings suggest that inflammation, rather than intrinsic secretion defects, may play a significant role in the pathophysiology of diabetes in this model.